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Possible Link Between SARS-Cov-2 Infection and Parkinson's Disease

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Possible Link Between SARS-Cov-2 Infection and Parkinson's Disease International Journal of Molecular Sciences Review Possible Link between SARS-CoV-2 Infection and Parkinson’s Disease: The Role of Toll-Like Receptor 4 Carmela Conte Department of Pharmaceutical Sciences, University of Perugia, via Fabretti, 06123 Perugia, Italy; [email protected] Abstract: Parkinson’s disease (PD) is the most common neurodegenerative motor disorder character- ized by selective degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain, depletion of dopamine (DA), and impaired nigrostriatal pathway. The pathological hallmark of PD includes the aggregation and accumulation α-synuclein (α-SYN). Although the precise mechanisms underlying the pathogenesis of PD are still unknown, the activation of toll-like receptors (TLRs), mainly TLR4 and subsequent neuroinflammatory immune response, seem to play a significant role. Mounting evidence suggests that viral infection can concur with the precipita- tion of PD or parkinsonism. The recently identified coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of ongoing pandemic coronavirus disease 2019 (COVID-19), responsible for 160 million cases that led to the death of more than three million individuals worldwide. Studies have reported that many patients with COVID-19 display several neurological manifestations, including acute cerebrovascular diseases, conscious disturbance, and typical motor and non-motor symptoms accompanying PD. In this review, the neurotropic potential of SARS-CoV-2 and its possible involvement in the pathogenesis of PD are discussed. Specifically, the involvement of the TLR4 signaling pathway in mediating the virus entry, as well as the massive immune and inflammatory response in COVID-19 patients is explored. The binding of Citation: Conte, C. Possible Link SARS-CoV-2 spike (S) protein to TLR4 and the possible interaction between SARS-CoV-2 and α-SYN between SARS-CoV-2 Infection and as contributing factors to neuronal death are also considered. Parkinson’s Disease: The Role of Toll-Like Receptor 4. Int. J. Mol. Sci. Keywords: Parkinson’s disease; SARS-CoV-2; COVID-19; toll-like receptor 4; synuclein; neuroinflam- 2021, 22, 7135. https://doi.org/ mation 10.3390/ijms22137135 Academic Editor: Maurizio Battino 1. Introduction Received: 20 May 2021 According to the World Health Organization (WHO), Parkinson’s disease (PD) is Accepted: 29 June 2021 Published: 1 July 2021 the second most common neurodegenerative disease in the world, after Alzheimer’s disease (AD), and one of the most common causes of neurological disability with a high Publisher’s Note: MDPI stays neutral social impact [1]. The prevalence of PD is about 10 million people worldwide, and it with regard to jurisdictional claims in is estimated that there will be about 13 million people with PD by 2040 [2]. PD is a published maps and institutional affil- chronic, progressive, age-related neurodegenerative disease clinically characterized by iations. motor symptoms, such as bradykinesia, rigidity, tremor at rest, slow movements, and postural instability [3]. Motor symptoms are the consequence of the progressive loss of neuromelanin-containing neurons, especially dopaminergic neurons (DA) in the substantia nigra pars compacta (SNpc) and dopamine depletion in the striatum, as confirmed by post- mortem study of clinically diagnosed PD patients [4,5]. The pathological hallmark of PD is Copyright: © 2021 by the author. Licensee MDPI, Basel, Switzerland. represented by the accumulation of cytoplasmic inclusions such as Lewy bodies (LB) and α α This article is an open access article Lewy neurites rich in -synuclein ( -SYN) [6–8]. distributed under the terms and Albeit a number of genetic and environmental risk factors have been characterized, conditions of the Creative Commons the cause(s) of PD are still unknown. In the last decades, studies have suggested the Attribution (CC BY) license (https:// association between certain viral infections and acute and chronic parkinsonism. Most creativecommons.org/licenses/by/ virus species include herpesvirus, Coxsackie, Japanese encephalitis B, Epstein Barr, Human 4.0/). Immunodeficiency Virus (HIV), and western equine encephalitis [9–17]. Int. J. Mol. Sci. 2021, 22, 7135. https://doi.org/10.3390/ijms22137135 https://www.mdpi.com/journal/ijms Int. J. Mol. Sci. 2021, 22, 7135 2 of 20 In the CNS, specialized innate immune sentinels, such as microglia, macrophages, dendritic cells, and astrocytes detect and clear viral agents by activating a robust immune response. However, many viruses use different strategies to elude immune system, cross the blood–brain barrier (BBB), and directly enter the nervous system. For example, viruses can enter the CNS via a “Trojan horse” mechanism using infected leucocytes as a vehicle for the passage from the blood through the BBB. [18]. Viruses may cause the disruption of the BBB integrity to gain access to the CNS [19]. Viral invasion of neural tissues can initiate inflammatory signaling by local primed immune cell recruitment, resulting in the release of abundant levels of an array of proinflammatory cytokines/chemokines that in turn can disrupt the BBB and increase its permeability [20]. The connection between systemic inflammation, PD, and neuroinflammation has been largely elucidated and a number of studies suggest that Toll-like receptors (TLRs), mainly TLR2 and 4, participate in the pathogenesis of PD as promoters of immune/neuroinflammatory responses that precede both motor and non-motor symptoms. The overexpression of TLR4 has been found in circulating monocytes of PD patients, in B cells, and in the caudate/putamen [21–24]. Studies in animal models of PD reported the potential role of TLR4 in mediating biochemical changes as well as dopaminergic cell death and α-synuclein accumulation in the midbrain [25,26]. Moreover, TLR4 has been found to play a critical role as a mediator of the neurotoxicity induced by α-synuclein oligomers [27]. Coronavirus disease (COVID-19) is an ongoing pandemic caused by a novel RNA (32 Kb genome) virus, namely, severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2), whose worldwide cases passed 160 million. COVID-19 deaths passed three million worldwide, and unfortunately these numbers are destined to further increase [28]. It is a highly transmissible virus strain of the recently discovered coronavirus in China and is transmitted primarily via respiratory droplets. It shares genetic identity with SARS-CoV and MERS-CoV [29,30]. It is composed of four major proteins named the spike (S), envelope (E), membrane (M), and nucleocapsid (N) [31]. All these proteins are notably implicated in viral infection, proliferation or host cell pathogenesis and are therefore predictable as the potential targets for vaccine or drug development. SARS-CoV-2 acts through the binding between the viral receptor S protein and differ- ent glycoprotein receptors on the cell surface. The virus S protein is a flexible and instable glycosylated complex. Recently, high-quality and stabilized forms of the trimeric S protein have been produced for use in vaccines and diagnostic tests [32]. A priming step of virus infection is represented by the cleavage of S protein by the transmembrane serine protease 2 (TMPRSS2) [33]. Then, cellular endocytosis occurs and RNA replication stages can take place. The main protein target on the cell surface is the angiotensin converting enzyme 2 (ACE2), an enzyme involved in converting angiotensin II to angiotensin. ACE2 is highly expressed in a wide variety of human tissues, including the brain [34–38]. SARS-CoV-2 has potential affinity to other candidate functional receptors such as dipeptidyl peptidase 4 [39], sialic acid residues on surface of airway cells and neurons [40], and lectin CD209L [41]. The respiratory tract is the first site that can be infected by SARS-CoV-2. If the virus is not cleared by the immune response, it reaches the lower respiratory tract and rapidly can be transmitted through droplets in a human-to-human manner [42]. COVID-19 includes a wide spectrum of clinical manifestations ranging from respiratory illness, with symptoms such as bronchitis, pneumonia, asthma, chronic obstructive pulmonary disease, and severe respiratory distress syndromes to multiorgan severe inflammation [43,44]. The high levels of cytokines secreted during the multisystem inflammatory syndrome can cause septic shock, sometimes fatal for the patients. Importantly, host response is fundamental to challenge the uncontrolled inflammatory response and plays a crucial role in susceptibility to SARS-CoV-2-mediated diseases [45]. Epidemiologic studies demonstrate that, unlike polio and others virus that evocate more severe complications for the young, SARS-CoV-2 infection is a zoonosis that affects Int. J. Mol. Sci. 2021, 22, 7135 3 of 20 older people, suggesting that age-associated chronic inflammation may occur with the development of disease [46]. A higher pathogenicity and death rate have been observed in particularly vulnerable and frail subjects and/or those affected by chronic inflammation or multiple comorbidities including diabetes, obesity, cardiovascular diseases, and immunosuppression [47–49]. Recent genome-wide association studies identified potential genetic factors involved in the development of COVID-19 [50]. Although the precise factors determining SARS-CoV-2 infection are poorly understood, systemic immune and hyperinflammatory responses play a major role. For example, it has demonstrated that the
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